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Sooyeon Lee

Researcher at Stanford University

Publications -  50
Citations -  4639

Sooyeon Lee is an academic researcher from Stanford University. The author has contributed to research in topics: Autophagy & Gene. The author has an hindex of 24, co-authored 44 publications receiving 3952 citations. Previous affiliations of Sooyeon Lee include Penn State Milton S. Hershey Medical Center & University of Florida.

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Lysosomal Proteolysis and Autophagy Require Presenilin 1 and Are Disrupted by Alzheimer-Related PS1 Mutations

TL;DR: It is shown that macroautophagy requires the Alzheimer's disease-related protein presenilin-1 (PS1) for v-ATPase targeting to lysosomes, lysOSome acidification, and proteolysis during autophagy, which represents a basis for pathogenic protein accumulations and neuronal cell death in AD.
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Autophagy Induction and Autophagosome Clearance in Neurons: Relationship to Autophagic Pathology in Alzheimer's Disease

TL;DR: It is shown that constitutive macroautophagy in primary cortical neurons is highly efficient, because newly formed autophagosomes are rapidly cleared by fusion with lysosomes, accounting for their scarcity in the healthy brain, and that the autophagic pathology observed in AD most likely arises from impaired clearance of AVs rather than strong autophagy induction alone.
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Lysosomal Proteolysis Inhibition Selectively Disrupts Axonal Transport of Degradative Organelles and Causes an Alzheimer's-Like Axonal Dystrophy

TL;DR: The AD-associated defects in neuronal lysosomal proteolysis are identified as a possible basis for the selective transport abnormalities and highly characteristic pattern of neuritic dystrophy associated with AD.
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Autophagy failure in Alzheimer's disease and the role of defective lysosomal acidification.

TL;DR: The most commonly used pH probes for sensitivity and localisation are evaluated, and LysoSensor yellow/blue‐dextran, among currently used probes, are identified as having the optimal profile of properties for measuring lysosomal pH.
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Intramuscular injection of α-synuclein induces CNS α-synuclein pathology and a rapid-onset motor phenotype in transgenic mice

TL;DR: This work shows that hind limb intramuscular injection of αS can induce pathology in the CNS in the human Ala53Thr (M83) and wild-type (M20) αS transgenic mouse models, and is the first evidence that an entire neurodegenerative proteinopathy associated with a robust, lethal motor phenotype can be initiated by peripheral inoculation with a pathogenic protein.